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CD4 + CD25 + regulatory T lymphocytes in allergy and asthma
Author(s) -
Shi H.Z.,
Qin X.J.
Publication year - 2005
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.2005.00844.x
Subject(s) - il 2 receptor , immunology , foxp3 , cytotoxic t cell , tumor necrosis factor alpha , immune system , cytokine , biology , medicine , t cell , in vitro , biochemistry
Allergic asthma is characterized by airway hyper‐responsiveness and chronic mucosal inflammation mediated by CD4 + Th2 lymphocytes. Regulatory CD4 + CD25 + T cells are important components of the homeostasis of the immune system, as impaired CD4 + CD25 + T cell activity can cause autoimmune diseases and allergy. The mechanism of suppression by CD4 + CD25 + T cells remains controversial; different in vivo and in vitro studies raise possible roles for the immunosuppressive cytokines interleukin‐10 and transforming growth factor‐ β , forkhead transcription factor Foxp3, glucocorticoid‐induced tumor necrosis factor receptor, cytotoxic lymphocyte associated antigen‐4, 4‐1BB costimulator receptor, a CD4‐related molecule LAG‐3, and neuropilin‐1. Current data suggest that Th2 responses to allergens are normally suppressed by CD4 + CD25 + T cells. Suppression by CD4 + CD25 + T cells is decreased in allergic individuals. Furthermore, CD4 + CD25 + T cells play a key role in regulating airway eosinophilic inflammation. The immunomodulatory properties of CD4 + CD25 + T cells do extend to Th2 responses, most notably by limiting the development of a proinflammatory CD4 + Th2 phenotype characterized by reduced cytokine production. An understanding of the roles of CD4 + CD25 + T cells in vivo could provide better insight into the design of novel approaches to modulate the chronic airway inflammatory reaction evident in bronchial asthma.